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H7N9 – Discussion, April 1, 2013 to June 3, 2013 (Closed)
While China is grappling with H7N9, here in EU pictures like this are circulating (A&E Crisis in UK, ????): xhttp://www.telegraph.co.uk/active/9967793/Crisis-hospital-sets-up-tent-for-AandE-patients.html
Reasons behind this overcrowded services is not clear... ???
HK SFH said that H7N9 virus gene sequences demonstrated that the virus has a 'signature' that indicates its ability to infect human. See main forum post... It remains sensitive to NAI drugs.
Details surfaced yesterday via genetic analysis:
Preliminary GeneWurx H7N9 Fatalities Overview - Version 2 Available
(1) A short deletion (69-73aa) in stalk region of NA protein.
(2) 627 E > K mutation in PB2 sequence, indicative of mammalian adaptation.
(3) Quite a few amino acid substitutions in NP protein. Interestingly,
a recent paper (Bogs et al. 2011) suggests PB2 627 mutation depends on the
origin of NP protein
UN health agency dismiss H7N9 bird flu pandemic fears
Published: 3 Apr 2013 at 19.49 Online news: Asia
...
"Given the fact that we've seen seven confirmed cases, plus there are reports of other cases, it would not be surprising to see additional cases," said Gregory Hartl, spokesman of the WHO's influenza and epidemics division.
"But these would be additional cases, one by one. We have no evidence so far of human-to-human transmission, and without human-to-human transmission, the likelihood or risk of pandemic is low," he told reporters.
"We're a long way away from thinking about a pandemic," he added.
... "There's no common factor for all the cases," Hartl noted.
...
All the latest top stories and breaking news. Thailand’s most credible source of Thai and international developments. In-depth business and political news, leading Lifestyle trends, broad international sports coverage, plus English language learning
Although there is limited evidence (the potential family cluster associated with the deceased 87 year old patient) for human to human transmission, I am concerned by this recent report of a new case-patient. I question the plausibility of this patient acquiring virus from animals while residing in a retirement home.
It is reassuring that no ill health care workers or other residents have been detected in an apparent group residential setting. It raises the issue of undefined host susceptibility factors.
?Patients Yang, male, 67 years old, Hangzhou, a retirement home. On March 25 because of cough, fever and other symptoms to stay at a hospital in Hangzhou, go to the Affiliated Hospital of Zhejiang University School of Medicine; April 2 rescue. In the afternoon of April 2, Zhejiang Province Center for Disease Control reports the patient's specimen test results for the H7N9 avian influenza virus nucleic acid positive.
April 3, the patient specimens were the China CDC influenza central laboratory for review of the H7N9 avian influenza virus nucleic acid positive.?
I have been having a look at the phyloginic trees (Cladograms) linked to in Gs's post #33. They are broadly in line with analysis on this thread.
They have highlighted A/brambling/Beijing/16/2012 (A/H9N2) as a good match on the internal genes particularly the polymerase complex components (PA, PB1 & PB2). These form a working unit and will often stay together in reassortments as mixing them up is likely to impair their function leaving the resultant strain less viable against existing wild types.
As Gs suggested in post #13 we may have a number of reassortments going on and the bramling's other internals are not quite as close a match but, as Mixin's BLASTs showed, even these were at least 97% homologous.
A/duck/Mongolia/119/2008 (A/H7N9) appears on both the HA and NA lists but is, as noted in my post #10, not as close but I was only looking a H7N9 candidates. The close matches on the H7 are ducks in Zhejiang and Korea and for the N9 strand a duck and some wild birds, also in Korea, so again in line with Gs's suggestion we are looking at a prior reassortment between these lines to form an H7N9 pairing which has not been caught and sequenced.
They also picked up and addressed Mixin's point about one of the 3 released sequences being a bit removed from the other two (see post #10 in this thread).
In all segments A/Shanghai/2/2013 groups with A/Anhui/1/2013 to the exclusion of A/Shanghai/1/2013 but in NP the common ancestor of the 3 is older suggesting perhaps a further reassortment of a more divergent NP gene at some point in one or other of the lineages. This suggests that the A/Shanghai/1/2013 sequence is may the result of a separate zoonosis from a bird lineage with a slightly divergent NP.
The graphic in post #23 in this thread shows the reassortment route that lead to H1N1(2009) and, hopefully, one day we will be able to generate a similar one for this flu.
Does silent virus in poultry occasionally infect humans?
The Associated Press Posted: Apr 3, 2013 12:04 PM ET
... "We speculate that when this virus is maintained in poultry the disease will not appear, and similar in pigs, if they are infected, so nobody recognizes the infection in animals around them, then the transmission from animal to human may occur," said Dr. Masato Tashiro, director of the World Health Organization's influenza research centre in Tokyo and one of the specialists who studied the genetic data. "In terms of this phenomenon, it's more problematic."
This behaviour is unlike the virus's more established relative, the virulent H5N1 strain, which set off warnings when it began ravaging poultry across Asia in 2003. H5N1 has since killed 360 people worldwide, mostly after close contact with infected birds.
"In that sense, if this continues to spread throughout China and beyond China, it would be an even bigger problem than with H5N1 in some sense, because with H5N1 you can see evidence of poultry dying, but here you can see this would be more or less a silent virus in poultry species that will occasionally infect humans," said University of Hong Kong microbiologist Malik Peiris, who also examined the information.
...
Scientists taking a first look at the genetics of the bird flu strain that recently killed two men in China said Wednesday that the virus could be harder to track than its better-known cousin H5N1 because it might be able to spread silently among poultry without notice.
There are lots of reassortments in H9N2, most of similar segments,
and the polymerases are separated too.
You can see it even in that small mutation table of best ~12 matches which I posted.
That table even has recombinations, which however often looked as errors in the past.
the number of nucleotide-differences in the 8 segments are:
S1-A1:7,14,3,12,35,9,1,2
S1-S2:9,14,3,13,35,9,1,2
(S1=Shanghai/1,A1=Anhui/1,S2=Shanghai/2)
clearly a new segment 5 was grasped and 2,4 look also different from 3,7,8
speculating about a possible reassortment timeline and trying
to make sense of the
7,14,3,12,35,9,1,2
9,14,3,12,35,9,1,2
differences between S1 and S2/A1
(mutation rate:
~6 nucleotides per year in 1,2,3,4
~4 in 5,6
~2 in 7,8)
so the first major wH7N9+pH9N2-->pH7N9 reassortment would have happened ~1 year ago
assuming that the virus is always much more prevalent in poultry than in wild birds or mammals
i.e. wrt. double infections
Nancy Cox:
...some molecular signs of possible adaptation in mammals...particular genetic
sequence indicates replication in domestic poultry not wild birds.
...mammalian receptors
its animal source is unknown. in birds or pigs or both, we don't rule out other sources
--------------------------------------------------------
WHO analysis:
signs of adaptation to growth in mammalian species,...bind to mammalian cells...
grow at mammalean temperature
ongoing H7N9 transmission
------------------------------------------------------------
Webby:
This thing doesn't any longer look like a poultry virus.It really looks to me like it's adapted in a
mammalian host somewhere.It's not clear what the mammalian host is, but the likeliest bets
are pigs and humans
------------------------------------------------------------
other experts quoted by Nature
genetic features suggesting that the virus is adapting to mammals
------------------------------------------------------------
Chinese officials and other experts:
the virus probably came from poultry
---------------------------------------------------------------
Peiris not mentioned,quoted
------------------------------------------------
adapting to mammals ? That seems to require a continuous spread
in mammalean hosts.
And in history that required a circulation of years, decades.
they suggest that the 3 marks : E627K(1),Q226L(4),deletion in NA [what else ?] did evolve
in mammals and are spreading ? Well, the deletion presumably does, E627K is
in the H5N1 Qinghai strain, Q226L is in 2 of 3 and often just evolved in the host
as did E627K.
--------------------------------------
I wished those experts would publically discuss with each olther in internet, as we do.
Instead they communicate less efficiently via press statements.
In formulations chosen so laymen journalists understand it.
In statement anxiously and carefully worded, not how you usually talk with friends,collegues in debates.
----------------------------------------
I also feel that the whole process of truth-seeking in flublogia is less advanced and productive
than what I used to see in math an computer forums before I entered flublogia.
Where are the expert flubies sitting together in one thread and discussing their theories ?
Some tweet, some collect news, some post press-releases, some post monologues in blogs
or forums that very few people read. Rarely you find them discussing with each other.
Merge the flubie communication gateways.
Reconstruction of the 1918 Influenza Virus: Unexpected Rewards from the Past
Jeffery K. Taubenbergera, David Baltimoreb, Peter C. Dohertyc, Howard Markeld, David M. Morense, Robert G. Websterf, and Ian A. Wilsong
"Although its origin has not been fully resolved (2, 24, 25), the avian influenza virus-like genome of the 1918 pandemic virus suggests derivation from an avian virus in the decade before 1918, with or without adaptation in an intermediate host (26). (Qi L, et al. 2012. Analysis by single gene reassortment demonstrates that the 1918 influenza virus is functionally compatible with a low pathogenicity avian influenza virus in mice. J. Virol. 86:9211?9220.)"
I don't know how they arrived at the decade for adaptation - and whether it actually caused illness prior to adaptation. Are there any similarities between initial 1918 genome and the current one? I.e., mammalian adaptation in the same areas - even though the virus is primarily avian?
it's the distance from the bird-index or avian consensus as they call it,
which suggests ~decade.
It's the amount of A,T nucleotides that grow over decades in mammals.
It's the normal influenza evolution rate with ~30-40 nucleotide mutations
per year in the genome , ~80% of which are synonymous.
It's the similarity between the human and swine linages related
to the 1918 virus. It's the distance to similar bird-strains
that were circulating later
How is it possible this virus can suddenly adapt to mammals?
Is this a precedence? or are there events that happened like this before - where the virus genetics indicate mammalian adaptation - suddenly - without a decade prior?
Did H5N1 have similar mammalian adaptation during the 1997 event? Since 2003?
Thank you for considering my questions. I am trying to understand the consistent references to the genetic adaptation.
we had these things before.
The Dutch vet with E627K comes to mind.
The deletions in NA and NS1 in H5N1.
some mutations at the RBD in H5N1
D225G in H1
but these usually were single events, now we have 3 things together.
But I think that's still a heap of single events, though more, and doesn't
imply evolution in mammals.
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